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Show Journal of Neuro- Ophthalmology 20( 4): 253- 258, 2000. 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Giant Cavernous Carotid Aneurysms: Clinical Presentation in Fifty- seven Cases Cecil D. Hahn, MD, David A. Nicolle, MB, ChB, FRCSC, FRCSE, FRCOpth, Stephen P. Lownie, MD, FRCSC, and Charles G. Drake, MD, FRCSC i • o i * • V Objectives: To review the presenting symptoms and ophthalmic findings of 57 patients with cavernous carotid aneurysms of giant size (> 2.5- cm diameter). Materials and Methods: Hospital charts of 57 patients with giant cavernous carotid aneurysms who presented to University Hospital in London, Ontario, Canada between 1961 and 1993 were reviewed. All patients were proven by cerebral angiography to have unruptured giant cavernous carotid aneurysms. Results: Forty- six patients ( 81%) were women ( mean age, 54 years). The most common presenting symptoms were diplopia ( 89%), retroorbital pain ( 61%), headache ( 19%), diminished or blurred vision ( 14%), and photophobia ( 4%). The most common clinical sign was partial or complete ophthalmoplegia ( 93%). Trigeminal nerve involvement was found in 37% of patients. Other clinical signs included ptosis, decreased visual acuity, proptosis, and visual field defects. Conclusions: This study characterizes a large group of patients with giant cavernous carotid aneurysms seen over a 30- year period at a single institution. As in previous studies, diplopia and retroorbital pain were the most common symptoms. The high incidence of ophthalmoplegia observed in this study may be explained by a greater compressive and/ or ischemic effect of giant aneurysms compared with their smaller counterparts. Key Words: Carotid artery diseases- Cerebral aneurysm- Internal carotid artery- Cavernous sinus- Ophthalmoplegia- Case series- Retrospective studies. Cavernous carotid aneurysms represent 2% to 5% of all intracranial aneurysms ( 1,2,3). They are distinct from other intracranial aneurysms in their anatomy, presentation, and clinical course. Arising from the intracavernous portion of the internal carotid artery, the aneurysmal sac is confined within the cavernous sinus, and it is separated from the subarachnoid space by the dural lining of the Manuscript received August 17, 1999; accepted February 1, 2000. From the Division of Neurology ( CDH), The Hospital for Sick Children and University of Toronto, Toronto, Ontario, Canada; and the Departments of Ophthalmology ( DAN), Clinical Neurological Sciences ( DAN, SPL, CGD), and Diagnostic Radiology, Division of Neuroradiology ( SPL), University of Western Ontario, London, Ontario, Canada. Address correspondence and reprint requests to D. A. Nicolle, MD, Department of Ophthalmology, London Health Sciences Centre, 339 Windermere Road, London, Ontario, N6A 5A5. cavernous sinus ( Figs. 1- 3). Cavernous carotid aneurysms classically present with local signs and symptoms including diplopia, retroorbital pain, headache, ptosis, proptosis, blurred vision, and facial anesthesia or paresthesia. The natural history of cavernous carotid aneurysms is variable, ranging from spontaneous remission to gradual symptomatic progression to rupture ( 4). Spontaneous rupture of an intracavernous aneurysm is rare, and it results in a carotid- cavernous fistula. The risk of subarachnoid hemorrhage from aneurysmal rupture is low, unless the aneurysm extends intradurally. Aneurysms of the cavernous sinus are classified according to their maximum diameter as small (< 1 cm), large ( 1- 2.5 cm), and giant > 2.5 cm). This study reviews the presenting symptoms and ophthalmic findings in a series of 57 patients with cavernous carotid aneurysms of giant size. METHODS Fifty- seven patients with giant cavernous carotid aneurysms were selected from a database of patients who presented to the neurosurgical service at University Hospital in London, Ontario, Canada between 1961 and 1993. Patient charts were reviewed for symptoms and clinical findings at presentation ( Table 1). All patients were admitted to the neurosurgery service, and many were also examined by an ophthalmologist in consultation. All patients included in this study were proven by cerebral angiography to have giant aneurysms with a diameter > 2.5 cm arising in the cavernous segment of the internal carotid artery, below the origin of the ophthalmic artery and beyond the petrous segment of the internal carotid artery. Patients were excluded from the study if there was any evidence of traumatic or mycotic etiology, if the aneurysm extended outside the cavernous sinus, or if the aneurysm had ruptured, creating a carotid-cavernous fistula. All patients underwent treatment by a combined team of neurosurgeons and interventional neuroradiologists ( Table 1). Treatments included application of a Selverstone clamp, ligation, or balloon occlusion of the proximal internal carotid artery. In addition, some patients received adjunctive extracranial- intracranial bypass of their internal carotid circulation ( 5). 253 254 C. D. HAHN ETAL. TABLE 1. Clinical presentation of 57 patients with giant cavernous carotid aneurysms Case 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 Initials AB AB AC AG AH BM BT BK CW CB CI DO DM DC DB DB DB DN DM EM HG HL HM IA JY JG JR LS LB LG MK MA MB MM Age 55 54 68 48 58 74 64 45 54 58 69 72 14 55 67 55 74 53 6 15 72 60 65 63 70 59 57 49 60 64 59 65 42 72 Sex F F F F F F F M F F M F M F F F F F M M M F F F F F F F F F F F F F Presenting symptoms Retroorbital pain, diplopia Retroorbital pain, ptosis, diplopia, blurred vision, V, hypalgesia Diplopia, retroorbital pain Diplopia, ptosis, miosis, retroorbital pain Diplopia Diplopia, retroorbital pain, headache Headache, diplopia, V2 analgesia, V2, V3 neuralgia Diplopia, retroorbital pain, headache, ptosis Retroorbital pain, diplopia, ptosis Diplopia, ptosis, headache, V, analgesia, V2 hypalgesia Retroorbital pain, diplopia, ptosis, V,, V2 hypalgesia Retroorbital pain, ptosis, diplopia Diplopia Retroorbital pain, diplopia, proptosis, V,, V2, V3 hypalgesia Retroorbital pain blurred vision, V,, V2 hypalgesia Diplopia, ptosis, mydriasis Diplopia, retroorbital pain Blurred vision, diplopia, ptosis Diplopia, retroorbital pain, V„ V2, V3 hypalgesia Blurred vision diplopia Diplopia, occipital headache Headache, diplopia, ptosis Diplopia, diminished vision Diplopia, headache, retroorbital pain Diplopia, ptosis, retroorbital pain Diplopia, ptosis, bilateral retroorbital pain Retroorbital pain, ptosis, diplopia Diplopia Diplopia, retroorbital pain, ptosis Diplopia, retroorbital pain, ptosis, proptosis, V,, V2 hypalgesia Diplopia, retroorbital pain, ptosis Diplopia, retroorbital pain, V2, V3 paresthesiae, bruit in ipsilateral ear Diplopia, V,, V2, V3 hypalgesia Retroorbital pain, ptosis, diplopia, V,, V2 hypalgesia V Visual acuity/ fields ^ Ipsilateral temporal hemianopia * Count fingers OU, ipsilateral central scotoma * Ipsilateral count fingers at 3 ft, contralateral 20/ 100 * * * 20/ 200 OU * 20/ 70 OU * 20/ 400 ipsilateral, 20/ 200 contralateral * * * III IV 0 0 • • • • • 0 • 0 0 o • • o 0 0 0 • • 0 0 0 0 VI o • • • 0 0 o 0 0 • • 0 0 0 • 0 • 0 • • o • 0 • 0 • 0 0 0 Treatment Balloon occlusion Balloon occlusion EC- IC, balloon occlusion Selverstone clamp Balloon occlusion Selverstone clamp Balloon occlusion EC- IC, balloon occlusion Selverstone clamp, then balloon occlusion EC- IC, balloon occulusion Selverstone clamp EC- IC, balloon occlusion Balloon occlusion EC- IC, Selverstone clamp EC- IC, ICA ligation, trapping Selverstone clamp Balloon occlusion Selverstone clamp Silk ligation ICA Balloon occlusion EC- IC, balloon occlusion Selverstone clamp Balloon occlusion Selverstone clamp Balloon occlusion Selverstone clamp Balloon occlusion EC- IC, balloon occlusion EC- IC, balloon occlusion Balloon occlusion EC- IC, balloon occlusion EC- IC, balloon occlusion Balloon trapping, then balloon occlusion Balloon occlusion / Neuro- Ophthalmol, Vol. 20, No. 4, 2000 GIANT CAVERNOUS CAROTID ANEURYSMS 255 TABLE 1. ( Continued) Case Initials Age Sex Presenting symptoms Visual acuity/ fields III IV VI Treatment 40 53 54 35 36 37 38 39 MA MS MB MA NR 59 47 53 27 41 F F F F F PA TW VH 28 41 42 43 44 45 46 47 48 49 50 51 52 PB PP PR PT RR RP RN SM SD SL SM TM 57 58 67 55 31 51 15 65 46 61 64 62 F F F F M F M F F F F M 56 67 M 55 56 57 WB WL XG 60 57 38 F M F Diplopia, ptosis, miosis Headache, diplopia, V, neuralgia, hypalgesia Frontal headache, nausea, vomiting, diplopia, ptosis Retroorbital pain, blurred vision Diplopia, retroorbital pain, ptosis, V, hypalgesia, photophobia, proptosis, blurred vision Headache, retroorbital pain, diplopia, ptosis, V,, V2 hypalgesia Diplopia Diplopia Diplopia, retroorbital pain, ptosis, V, paresthesia Retroorbital pain, blurred vision Retroorbital pain, diplopia Retroorbital pain, ptosis, RAPD, V, analgesia, V2 hypalgesia and motor paralysis Retroorbital pain, diplopia Diplopia, ptosis, proptosis, V, neuralgia, V,, V2 hypalgesia Diplopia, V[ analgesia Diplopia, retroorbital pain, V, hypalgesia, paresthesiae Diplopia Diplopia, retroorbital pain, ptosis Diplopia, retroorbital pain, ptosis, V,, V2, V3 hypalgesia, motor paralysis Headache, retroorbital pain, ptosis, V,, V2 hypalgesia Retroorbital pain, photophobia Diplopia, ptosis Diplopia O Balloon occlusion • Balloon occlusion • Balloon occlusion EC- IC, balloon occlusion • Balloon occlusion Balloon occlusion O Balloon occlusion Balloon occlusion * * * * * * * 20/ 200 ipsilateral 2040 ipsilateral Ipsilateral inferior altitudinal defect Count fingers at 3 ft OU, ipsilateral superotemporal quadrantanopia O O • • 0 0 • • • • 0 0 • • • • • • • • • o • • • 0 • • • • Balloon occlusion ICA clip trappings Selverstone clamp EC- IC, balloon occlusion Selverstone clamp Balloon occlusion Selverstone clamp Balloon occlusion Balloon occlusion EC- IC, balloon occlusion Detached balloon occlusion Balloon occlusion Detached balloon occlusion Selverstone clamp * Sensory and/ or motor involvement of cranial nerve five. O Partial paresis of cranial nerves three, four, and six. • Complete paresis of cranial nerves three, four, and six. V, trigeminal nerve divisions one ( V,), two ( V2), and three ( V3); III, cranial nerve three; IV, cranial nerve four; VI, cranial nerve six; VA, visual acuity; EC- IC, extracranial- intracranial bypass; ICA, internal carotid artery; RAPD, relative afferent pupillary defect. RESULTS Complete results are summarized in Table 2. Patient Characteristics Of the 57 patients with giant cavernous carotid aneurysms, 46 patients ( 81%) were women and 11 patients ( 19%) were men ( mean age, 54 years). The youngest patient was a 6- year- old boy, and the oldest patient was a 74- year- old woman. The most commonly seen group was middle- aged to elderly women. In the pediatric population ( patients younger than 18 years), all four patients were male. Presenting Symptoms The most common presenting symptom was diplopia, seen in 51 patients ( 89%). Retroorbital pain was reported by 35 patients ( 61%). Headache ( defined as pain that was not specifically retroorbital) was reported by 11 patients ( 19%). Diminished or blurred vision was reported by eight patients ( 14%), and photophobia was reported by two patients ( 4%). Clinical Signs at Presentation The most common clinical sign at presentation was ophthalmoplegia, which was seen in 53 patients ( 93%), of which 44 ( 77%) had partial ophthalmoplegia and nine / Neuro- Ophthalmol, Vol. 20, No. 4, 2000 256 C. D. HAHN ET Ah. TABLE 2. Summary of presenting signs and symptoms Patient characteristics No. patients Sex F M Age ( y) Mean 54 Minimum 6 Maximum 74 Presenting symptoms Diplopia Retroorbital pain Headache Diminished or blurred vision Photophobia Clinical signs Ptosis Decreased visual acuity Proptosis Visual field defect Ophthalmoplegia Partial Complete Paresis of cranial nerves III, IV, VI III IV VI III only IV only VI only III and IV only III and VI only IV and VI only II, IV, and VI Dysfunction of cranial nerve V Ophthalmic division ( V,) Hypalgesia Neuralgia Paresthesia Maxillary division ( V2) Hypalgesia Neuralgia Paresthesia Mandibular division ( V3) Hypalgesia Neuralgia Paresthesia Motor paralysis No. patients 57 46 11 51 35 11 8 2 29 7 4 4 53 44 9 31 14 46 6 0 22 1 11 0 13 21 19 18 2 2 15 14 1 1 4 1 1 2 % 81 19 89 61 19 14 4 51 12 7 7 93 77 16 54 25 81 1 0 39 2 19 0 23 37 33 32 4 4 26 25 2 2 7 2 2 4 ( 16%) had complete ophthalmoplegia. Ophthalmoplegia was associated with third cranial nerve paresis in 31 patients ( 54%), with fourth cranial nerve paresis in 14 patients ( 25%), and with sixth cranial nerve paresis in 46 patients ( 81%). Isolated third cranial nerve paresis was present in six patients ( 11%), and isolated sixth cranial nerve paresis was present in 22 patients ( 39%). No patients demonstrated isolated fourth cranial nerve paresis. Combined paresis of cranial nerves three, four, and six was seen in 13 patients ( 23%). Combined paresis of cranial nerves three and six alone was seen in 11 patients ( 19%). Combined paresis of cranial nerves three and four alone was seen in one patient ( 2%). No patients demonstrated combined involvement of cranial nerves four and six alone. The trigeminal nerve was affected in 21 patients ( 37%). The ophthalmic division ( Vx) was involved in 19 patients ( 33%), the maxillary division ( V2) in 15 patients ( 26%), and the mandibular division ( V3) in six patients ( 11%). The most common sensory abnormality was hypalgesia or analgesia ( decreased or absent pain sensation). On occasion, neuralgia ( unprovoked pain sensation) and paresthesia ( abnormal sensation) were also seen in various branches of the trigeminal nerve distribution. Paralysis of the muscles of mastication ( V3) was present in two patients ( 4%). Ptosis was a presenting sign in 29 patients ( 51%), and decreased visual acuity was seen in seven patients ( 12%). Proptosis was present in four patients ( 7%), and visual field defects were found in four patients ( 7%). DISCUSSION Several previous studies ( 6,7,8) documented the clinical presentation of cavernous carotid aneurysms of mixed size, and one study focused on cavernous carotid aneurysms of giant size ( 9). To our knowledge, the current study represents one of the largest reported series of patients with giant cavernous carotid aneurysms. These patients were seen in a single institution, which permitted comprehensive selection of patients and systematic analysis of clinical records. The patients reviewed in this study represent a highly select group, many of whom were referred to this center because of its expertise in the treatment of giant aneurysms. Most patients sought treatment at a time when noninvasive neuroimaging techniques, including computed tomography ( CT) and magnetic resonance imaging ( MRI), were not yet available. As a result, all patients in this study were symptomatic at presentation, in contrast to other case series that have included asymptomatic patients whose cavernous carotid aneurysms were identified incidentally by CT or MRI. We used caution when comparing this study to previous case series of cavernous carotid aneurysms because each series differs in its method of patient selection and in its definition of clinical symptoms ( such as " headache" versus " retroorbital pain"). The characteristics of our patient group were very similar to those reported in previous case series. The great majority of our patients ( 81%) were women, and the mean age for both sexes was 54 years; these statistics are in agreement with previously reported associations of cavernous carotid aneurysms with women and with advancing age ( 6,8,10). We summarized our patients' signs and symptoms by specific categories to facilitate comparison with other studies. Diplopia and retroorbital pain were by far the most common presenting symptoms in our patient group. Ophthalmoplegia was by far the most common presenting sign; it was present in 93% of our patients. Ophthalmoplegia was more commonly partial than complete, and in agreement with previous observations ( 6), cranial nerve six was most commonly involved ( 81%), followed by cranial nerves three ( 54%) and four ( 25%). Ptosis was the second most common sign, present in 51% of patients. J Neuro- Ophthalmol, Vol. 20, No. 4, 2000 GIANT CAVERNOUS CAROTID ANEURYSMS 257 r L. FIG. 1. Anterior ( A) and lateral ( B) projections of a left internal carotid artery injection angiogram in a patient with a left giant cavernous carotid aneurysm. J A possible correlation between the size of cavernous carotid aneurysms and the severity of their clinical presentation has been a matter of debate. Linskey et. al. ( 6), in a study of 37 patients with mixed- size cavernous carotid aneurysms, reported no correlation between aneurysm size and the severity of symptoms. However, Ku-persmith et. al. ( 7), in a study of 70 patients with mixed-size cavernous carotid aneurysms, found that only patients with aneurysms of giant size presented with ophthalmoplegia. We found that our patients with giant aneurysms had a higher incidence of ophthalmoplegia ( 93%) than was reported in previous studies of mixed-size aneurysms. This observation supports the hypothesis that giant aneurysms may cause more symptoms than their smaller counterparts, possibly due to a greater ischemic and/ or greater compressive effect on cranial nerves traversing the cavernous sinus ( 11,12). FIG. 2. Axial magnetic resonance angiography partition images Demonstrating a left giant cavernous carotid aneurysm in the same patient as in Figure 1, after carotid occlusion treatment. The treatment of giant cavernous carotid aneurysms has evolved considerably since the first patients in this study were seen ( 13,14,15). Traditionally, the treatment of cavernous carotid aneurysms was controlled occlusion of the internal carotid artery in the neck. In the early 1900s, this was accomplished by ligature or by fascial bands; since the 1950s, this was accomplished with metallic clamps designed by Crutchfield and Selverstone ( 16,17). In some cases, extracranial- to- intracranial bypass surgery was undertaken to augment the cerebral collateral circulation ( 5). In the 1960s, the use of balloon- mounted catheters began, and by the late 1970s, detachable balloons of silicone or latex had been developed ( 1,18). Rapid advances in endovascular treatment over the past 10 years have opened up further options for the treatment of these aneurysms, including detachable platinum coils ( 19). All of the patients described in this study were treated using ligation, Selverstone clamping, or balloon occlusion of the proximal internal carotid artery, combined at times with extracranial- intracranial bypass. We are unable to comment on the clinical outcomes of these patients because most were referred to this center for treat- FIG. 3. Anterior projection of a magnetic resonance angiogram demonstrating a left giant cavernous carotid aneurysm in the same patient as in Figure 1, after carotid occlusion treatment. J Neuro- Ophthalmol, Vol. 20, No. 4, 2000 258 C. D. HAHNETAL. ment and were subsequently followed elsewhere. However, a survey of postoperative clinical notes indicates that many patients experienced immediate improvement in their symptoms after surgical treatment. Recent studies ( 4,7) demonstrated the benign natural history of these aneurysms and have argued for a more conservative approach to their treatment. Treatment is now commonly reserved for patients with intolerable pain, progressive ophthalmoplegia or visual loss, evidence of intradural extension or radiographic enlargement, and subarachnoid hemorrhage or epistaxis. To our knowledge, this study represents one of the largest reported series of patients, seen over a 30- year period in a single institution, with giant cavernous carotid aneurysms. 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